Poultry and meat are frequent sources of foodborne disease organisms. The pathogens associated with poultry products include Salmonella spp., Listeria monocytogenes, Escherichia coli and Campylobacter jejuni. These microorganisms are introduced into poultry and animal flocks during raising and onto carcasses during processing. These bacteria colonize the mucus covering gut surfaces and can also be found in deep mucus of intestinal crypts. The bacterial surfaces have specific adhesins or insertional structures which attach to the caudal ileum and ceca, and thereby resist abrasive loss by food materials which transit the intestine.
A variety of chemical agents and physical processes have been employed, with varying success, to remove and/or destroy some of the pathogenic organisms which transfer to meat and poultry surfaces during the processing of their carcasses. These include trisodium phosphate, chlorine, chlorine dioxide, organic acids, hydrogen peroxide, acidified sodium chlorite and steam. Despite the intervention of these materials and processes, for example, it is estimated that close to 25% of current poultry carcasses that reach US consumers contain Salmonella organisms. A number of recent outbreaks of infections and death caused by the specific E. coli strain 0157:H7 have occurred, as a result of contaminated beef.
Recent attention has been directed to reducing the colonization of poultry intestinal tracts by these pathogens, so that the subsequent processing of their carcasses would not be burdened with the elimination of their current high numbers. One such approach has been termed mucosal competitive exclusion, which involves feeding new chicks bacterial cultures derived from mucosa-associated microorganisms of chicken cecal epithelia in order to surpress the growth of pathogens such as Campylobacter and Salmonella in their gut. In one evaluation of this concept, chicks that had been exposed to this bacterial combination grew to yield processed carcasses in which only 10 percent were Salmonellae positive, as compared with 41 percent for untreated flocks. In another study, the reduction was from 9.1 percent Salmonella contamination of control carcasses to 4.5 percent for treated flocks.
In a related approach, it has been discovered that the inclusion of certain monomeric and dimeric sugars in the poultry diet will reduce the levels of Salmonella organisms that colonize their gut. As previously indicated, sugar receptors on the surfaces of intestinal epithelial cells apparently serve as receptors for the binding of some bacterial pathogens. The interaction between the Gram-negative bacterial pili and these receptor can be blocked by certain simple sugars in the animal feed. When 2.5% levels of arabinose, galactose, and lactose were included in the diet of chicks, there was a significant reduction in Salmonella levels in their cecal contents up through 21 days of age, except for lactose where organism levels reverted thereafter. An earlier study showed 5% dietary levels of these sugars to be very effective. In an in vitro study, the ceca of 1-week old chicks showed reduced bacterial adhesion when contacted by the carbohydrates D-galactose, N-acetyl-D-galactosamine, L-fucose, L+arabinose and D+mannose, but this effect disappeared in 2-week old chick ceca. Finally when 1-day old chicks were fed a 2.5% mannose solution for 10 days, and then challenged with Salmonella typhimurium, only 31% on average showed cecal contamination, compared with an average of 84% of control birds that were not first exposed to the sugar. Another study showed that the adherence of the pathogen Escherichia coli to mucosal epithelial cells of mammals is mediated by mannose-specific sites on the bacterial surface, and that inclusion of mannose in the diet will interfere with E. coli adherence to the mammalian epithelial cells.
An adaptation of the use of simple dietary sugars for reducing Salmonella populations in poultry intestinal tracts has appeared recently in the inclusion of dried yeasts in poultry diets. Yeast cell walls include polymeric sugars such as mannans and galactomannans in their compositions, which polymers apparently function in the same manner as their component sugars, i.e. in attaching to the bacterial sites which would otherwise bind to intestinal surfaces. The disadvantage of this approach, of course, lies in the cost-inefficiency associated with use of whole yeast cells as a carrier for the specific sugar components that are present only on the yeast cell surfaces. The more the weight requirement of the feed ingredient, the more costly is the diet, as well as the possibility that the other yeast components may have adverse effects on poultry nutrition. In a recent study, dried yeast cells that were incorporated into chicks' diets were found to bring about a significant reduction in Salmonella levels of the animals' ceca.
The present invention results from an attempt to understand and identify the specificity of the binding sites associated with certain pathogen surfaces, which binding site are apparently associated with certain carbohydrate structures, and to then apply this knowledge in order to optimize the selection of those carbohydrates which most effectively and economocially reduce the levels of human pathogens in animal viscera.